This study investigated the role of miR-214 in modulating proliferation and invasion of human colon cancer SW620 cells. Fifty-five patients with colon cancer who were treated in China-Japan Union Hospital of Jilin University from March 2014 to March 2015 were enrolled into this study. Their cancer and corresponding paracancerous tissues were collected and the expression levels of miR-214 were determined by RT-qPCR. A miR-214 expression vector was constructed. SW620 cells were transfected with the miR-214 expression vector and a blank vector. Cells transfected with the miR-214 expression vector were assigned to the miR-214 positive group and cells transfected with the blank vector were assigned to the miR-214 negative group. Cell proliferation, invasion and apoptosis were assessed by MTT assay, Transwell migration assay and TUNEL apoptosis assay, respectively. The RT-qPCR results showed that the expression level of miR-214 in colon cancer tissue, as well as in miR-214 negative cells, was significantly lower than that in paracancerous tissue (P<0.05 for both). In cell comparison, the expression level of miR-214 in the miR-214 positive group was significantly higher than that in the miR-214 negative group (0.483±0.001 vs. 0.172±0.001; P<0.05). The proliferation level of SW620 cells in the miR-214 positive group was lower than that in the miR-214 negative group (P<0.05). The Transwell migration assay indicated that there were less cells penetrating the membrane in the miR-214 positive group than in the miR-214 negative group (P<0.05). In addition, The apoptosis rate of cells in the miR-214 negative group was significantly lower than that in the miR-214 positive group (P<0.05). Finally, the low expression of miR-214 was found in colon cancer, indicating that miR-214 is a cancer suppressor playing an opposing role in colon cancer onset and progression. Therefore, miR-214 can promote apoptosis of colon cancer cells SW620 by inhibiting their proliferation and invasion.
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| http://dx.doi.org/10.3892/ol.2018.9521 | DOI Listing |
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